The multiple fault T-lymphocyte effector functions in systemic lupus erythematosus may result from altered signal transduction with a defective biochemical pathway(s). Impaired cAMP-inducible, protein kinase A(PKA) dependent protein phosphorylation in intact T-lymphocytes from subjects with mild to severe SLE due to deficient activity of the Type 1 isozyme of PKA(PKA-1) have been demonstrated. Dr. Kammer seeks to define the biochemical, molecular and genetic mechanisms leading to diminished PKA-1 phosphotransferase activity.